Cadmium (Cd) is a highly toxic substance in the aquatic ecosystem, which can represent a high risk to fish. Fish are exposed to heavy metals through waterborne and dietary pathways, some of which are absorbed by the body and can accumulate in specific tissues without being eliminated. The accumulation varies depending on several factors such as dose, exposure route, exposure time, metal types, and biological status of the fish, and environmental parameters such as DO, salinity, pH, and metal speciation. As Cd speciation occurs in the water, the amount accumulated in the fish can vary, and consuming Cd-accumulated fish can pose a risk to human health. Cd introduced into the body of fish can directly affect blood properties through the circulatory system. Cd introduced into the circulatory system of fish can reach all tissues through the blood flow, and the accumulation of specific tissues is different depending on the blood flow by the energy and oxygen demand of each tissue. Therefore, this review aimed to determine the toxic effects of Cd exposure in fish and identify indicators to assess the extent of Cd bioaccumulation toxicity in fish induced by Cd exposure.

Juvenile Paralichthys olivaceus were exposed to waterborne hexavalent chromium at various concentrations (0, 0.5, 1.0, and 2.0 mg/L) for 10 days. After chromium exposure, the activities of superoxide dismutase and glutathione S-transferase, which are oxidative stress indicators, were significantly increased; however, the glutathione level was significantly reduced. Acetylcholinesterase activity as a neurotoxicity marker was significantly inhibited upon chromium exposure. Other stress indicators, including plasma cortisol and heat shock protein 70, were significantly increased. The immune response markers (lysozyme and immunoglobulin M) were significantly decreased after chromium exposure. These results suggest that exposure to environmental toxicity in the form of waterborne chromium at concentrations higher than 1.0 mg/L causes significant alterations in antioxidant responses, neurotransmitters, stress, and immune responses in juvenile olive flounders. This study will provide a basis for an accurate assessment of the toxic effects of hexavalent chromium on aquatic organisms.

Cadmium (Cd) is a non-essential trace element that poses significant toxic effects on fish. This review focuses on hematological and plasma biochemical parameters as key indicators of fish health under Cd exposure. Hematological parameters, such as red blood cell (RBC) count, hemoglobin (Hb) concentration, and hematocrit (Ht), were selected for their critical role in oxygen transport and their sensitivity to Cd-induced disruptions, which often result in anemia and impaired oxygen delivery to tissues. Mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), and mean corpuscular hemoglobin concentration (MCHC) provide further insights into erythropoiesis and hemoglobin synthesis, both of which are essential for assessing Cd toxicity. Plasma biochemical parameters, including calcium, magnesium, glucose, cholesterol, total protein, and liver enzymes such as aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP), are crucial for understanding ionic balance, metabolic regulation, and organ function, especially in fish exposed to Cd. These biomarkers offer a comprehensive view of the physiological stress and organ damage caused by Cd toxicity. This review synthesizes literature findings on the toxic effects of Cd on these parameters. It also discusses potential mitigation strategies, including dietary supplementation with antioxidants and trace elements, to counteract the harmful effects of Cd exposure.

In this study, gametotoxicity and embryotoxicity experiments were performed using Hemicentrotus pulcherrimus to investigate the toxic effects of tributyltin (TBT). The effects of TBT on fertilization and embryogenesis were assessed at various concentrations (0, 0.02, 0.05, 0.09, 0.16, 0.43, 0.73, 4.68, and 9.22 ppb). The fertilization rates decreased in a concentration-dependent manner, with significant reduction following treatment with TBT at 0.05 ppb. Embryos exhibited developmental impairment after TBT exposure at each tested concentration. The frequency of developmental inhibition delay that treatment with TBT delayed embryonic development in a dose-dependent manner, with 100% of embryos exhibiting developmental impairment at 4.68 ppb. During developmental recovery tests, embryos cultured in fresh media without TBT showed advanced embryonic development. Although the observed normal development after transferring the developmentally delayed embryos to fresh media without TBT offers prospects for the restoration of contaminated environments, embryonic development remained incomplete. These results suggest that TBT adversely affects the early embryonic development of H. pulcherrimus.